Administration of phosphatidylcholine–cholesterol liposomes partially reconstitutes fat absorption in chronically bile-diverted rats
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Background and aims: Intestinal bile deficiency in cholestatic patients leads to fat malabsorption. We addressed the potency of model bile, bile salts and phosphatidylcholine (PC)–cholesterol (CH) liposomes to reconstitute fat absorption in permanently bile-diverted (BD) rats. Methods: The plasma appearance of 13C-labeled palmitic acid (13C-16:0) and linoleic acid (13C-18:2) was determined after their enteral administration to BD or to control rats with an intact enterohepatic circulation (EHC) (13C-16:0 and 13C-18:2 dissolved in 25 % olive oil–75 % medium chain triacylglycerol oil mixture). BD rats were intraduodenally infused with buffer, model bile [consisting of 60 mM taurocholate (TC), 8 mM PC and 1 mM CH], buffer with TC, buffer with PC and CH liposomes, or buffer with lyso-PC and CH. Results: Plasma concentrations of 13C-16:0 and 13C-18:2 were consistently three- to eightfold higher in control rats than those in buffer-infused BD rats (P<0.01). ID administration of either model bile or TC to BD rats restored plasma appearance of 13C-fatty acids at least to concentrations observed in control rats. Administration of PC+CH liposomes to BD rats partially reconstituted the plasma appearance of 13C-16:0, but did not affect that of 13C-18:2. Compared with control rats, the area under the curve (AUC) of plasma 13C-16:0 concentrations was 13.0±6.9 % in buffer-infused rats and 40.9±3.1 % in liposome-infused rats (P<0.005). Conclusions: Enteral administration of PC+CH liposomes to BD rats partially corrects the absorption of palmitic acid. Present data suggest that administration of PC+CH liposomes could enhance fat absorption in clinical conditions of cholestasis in which bile salt supplemention is contraindicated.

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